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Published on: January 10, 2025
Δ9-Tetrahydrocannabinol (Δ9-THC) Improves Ischemia/Reperfusion Heart Dysfunction and Might Serve as a
Marta Banaszkiewicz1, Paulina Tarwacka1, Anna Krzywonos-Zawadzka1
1Division of Clinical Chemistry and Laboratory Hematology, Department of Medical Laboratory Diagnostics, Faculty of Pharmacy with Division of Laboratory Diagnostics, Wroclaw Medical University, 50-556 Wroclaw, Poland.
Insights
Delta-9-tetrahydrocannabinol (Δ9-THC) protects the heart from ischemia/reperfusion (I/R) injury by improving cardiac function and reducing cell damage. This study suggests Δ9-THC as a potential cardioprotective agent against I/R-induced heart dysfunction.
Area of Science:
- Cardiovascular Science
- Pharmacology
- Cell Biology
Background:
- Ischemia/reperfusion (I/R) injury is a significant clinical issue, often leading to organ damage via oxidative stress and inflammation.
- Reactive oxygen species (ROS) generated during I/R contribute to endothelial dysfunction and cellular damage.
- Delta-9-tetrahydrocannabinol (Δ9-THC), a cannabis compound, is recognized for its anti-inflammatory properties.
Purpose of the Study:
- To investigate the potential cardioprotective effects of Δ9-THC against cardiovascular dysfunction caused by I/R injury.
- To evaluate the impact of Δ9-THC on cellular viability, damage markers, and oxidative stress in cardiac tissue subjected to I/R.
Main Methods:
- Utilized isolated rat hearts (Langendorff method) and human cardiac myocytes (HCM) models.
- Applied an ex vivo/in vitro I/R protocol with and without Δ9-THC treatment.
- Measured key parameters including cell viability, lactate dehydrogenase (LDH) activity, ceramide kinase (CERK) activity, ROS levels, total antioxidant capacity (TAC), and hemodynamic function.
Main Results:
- Δ9-THC treatment significantly improved the recovery of cardiac function (p < 0.05).
- Reduced cell injury and decreased cell death were observed in Δ9-THC treated groups (p = 0.019 and p = 0.005, respectively).
- Δ9-THC administration normalized CERK levels, decreased ROS, and enhanced TAC in cardiomyocytes under I/R conditions.
Conclusions:
- Δ9-THC demonstrates significant cardioprotective effects by enhancing cardiomyocyte viability, improving metabolic activity, and reducing cellular damage.
- Δ9-THC restores heart mechanical function, positioning it as a potential therapeutic agent for I/R injury.
- The study proposes the administration of Δ9-THC prior to I/R events to mitigate cardiac damage.
Background:
Ischemia/reperfusion (I/R) is a pivotal mechanism of organ injury during clinical stetting for example for cardiopulmonary bypasses. The generation of reactive oxygen species (ROS) during I/R induces oxidative stress that promotes endothelial dysfunction, DNA dissociation and local inflammation. In turn, those processes induce cytokine release, resulting in damage to cellular structures and cell death. One of the major psychoactive compounds of Cannabis is delta-9-tetrahydrocannabinol (Δ9-THC), which is known as an anti-inflammatory mediator. Our research aimed to test if Δ9-THC may be protective in the treatment of cardiovascular system dysfunction arising from I/R heart injury.
Methods:
Two experimental models were used: isolated rat hearts perfused with the Langendorff method and human cardiac myocytes (HCM) culture. Rat hearts and HCM underwent ex vivo/chemical in vitro I/R protocol with/without Δ9-THC treatment. The following parameters were measured: cell metabolic activity, morphology changes, cell damage as lactate dehydrogenase (LDH) activity, ceramide kinase (CERK) activity, ROS level, total antioxidant capacity (TAC) and heart hemodynamic parameters.
Results:
Δ9-THC protected the heart, as evidenced by the improved recovery of cardiac function (p < 0.05, N = 3-6). Cells subjected to I/R showed lower cytoplasmic LDH activity, and 10 μM Δ9-THC treatment reduced cell injury and increased LDH content (p = 0.019, N = 6-9). Morphology changes of HCM-spherical shape, vacuolisation of cytoplasm and swollen mitochondria-were inhibited due to Δ9-THC treatment. I/R condition affected cell viability, but 10 μM Δ9-THC decreased the number of dead cells (p = 0.005, N = 6-9). The total level of CERK was lower in the I/R group, reflecting oxidative/nitrosative stress changes. The administration of Δ9-THC effectively increased the production of CERK to the level of aerobic control (p = 0.028, N = 6-9). ROS level was significantly decreased in I/R cells (p = 0.007, N = 6-8), confirming oxidative stress, while administration of 10 μM Δ9-THC enhanced TAC in cardiomyocytes subjected to I/R (p = 0.010, N = 6-8).
Conclusions:
Δ9-THC promotes the viability of cardiomyocytes, improves their metabolic activity, decreases cell damage and restores heart mechanical function, serving as a cardioprotective. We proposed the use of Δ9-THC as a cardioprotective drug to be, administered before onset of I/R protocol.
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